I have bee suffering from severe symptoms of post concussion syndrome for several.months after a car accident. The use of TB500 has been the only trratment ease my symptoms and give me my life back. I ceased use last week after 3 weeks and had reoccuring concussion symptoms. As such? I recommenced injections as of last night. Have you read much about the impact of TB500 on brain injury as I’d love to know if more prolonged use would have a permanent impact/remedy for me? Thanks for your time and interest.
To determine the effects of Tβ4 peptide and H2O2 on cytotoxicity, its cell viability was evaluated. A 48-h exposure to 0.1–5 μg/mL Tβ4 peptide did not affect H2O2-mediated cell viabilities (Fig 2A). In order to examine whether Tβ4 peptide suppressed ROS-induced inflammatory mediators, the ability of Tβ4 peptide on production of NO and PGE2, and expressions of COX-2 and iNOS were measured by RT-PCR, Western blot, and ELISA. Pretreatment with Tβ4 peptide dose-dependently inhibited H2O2-induced mRNA and protein expressions of COX-2 and iNOS, and NO and PGE2 production (Fig 2B–2E).

Melanotan II is a synthetic analogue of the α-melanocyte stimulating hormone (α-MSH). α-MSH is a melanocortin I receptor agonist which has a role in human pigmentation by stimulating production of eumelanin. Melanotan II was originally developed as a treatment for sexual dysfunction. However, the proposal was abandoned when development of the metabolite bremelanotide was established.

Thymosin β4 (TMSB4X, Tβ4) is the most abundant G-actin binding peptide of the cytosol and is a potent proangiogenic factor. The role of myocardin-related transcription factors (MRTF) and serum response factor (SRF) for this function was examined in experimentally induced prolonged ischemic myocardium areas of transgenic pigs ubiquitously and constitutively overexpressing Tβ4 driven by the cytomegalovirus promoter. Upon induction of a reversible loss of cardiomyocyte function which is amenable to therapeutic neovascularization, transgenic pigs did not experience a significant loss of perfusion nor myocardial function at rest or under rapid pacing. Functional vascular regeneration by induced capillary growth and maturation was found in the transgenic pigs (Hinkel et al., 2014).
People are using 5-HTP for absolutely everything from sleep disorders to OCD symptoms. After asking people in mental health Facebook groups whether they used it and why, I was inundated with responses. Sach Tennant, from London, takes it for her PMDD (premenstrual dysphoric disorder). "I only take it when I feel low and it only takes one hour to feel calm," she told me. "This month I only needed one to feel better. I don't get the zombie antidepressant feeling – you still have your emotions. Sleep is good on it. I used to have an inner voice that was male and used to bully me during PMT time. Noises seemed too loud, even like somebody eating a bag of crisps. Topping up with 5-HTP has stopped all this."
So far, few studies have definitively linked autism to problems in oxytocin signalling. Some of the clearest evidence emerged in February, from a team led by neurogeneticist Daniel Geschwind of the University of California, Los Angeles. The group showed that mice that lacked a working copy of the Cntnap2 gene — which has been implicated in a small subset of human autism cases — had fewer oxytocin-containing neurons in the hypothalamus and socialized less with other mice than did control mice15. After receiving doses of oxytocin every day for two weeks, the mice behaved normally again. “Until this, there was no evidence that there was a subtype of autism that had to do with oxytocin deficits,” Geschwind says.
20 patients (nine from the 5-HTP group and 11 from the Placebo group) completed the study. Brain tryptophan availability in diabetic patients was significantly reduced when compared to a group of healthy controls. Patients receiving 5-HTP significantly decreased their daily energy intake, by reducing carbohydrate and fat intake, and reduced their body weight.”
Young says that the oxytocin field would benefit from closer collaboration between basic and clinical researchers. If basic scientists can work out how oxytocin helps the brain to process social stimuli, then that might help in the design of stimuli — in the form of behavioural therapies — that could be given alongside the hormone to change behaviour, just as oxytocin and pup calls together affect virgin mice. “I think in the future these two branches need to have more communication,” Young says.

5-HTP (5-Hydroxytryptophan) is a chemical by-product of the protein building block L-tryptophan. It is also produced commercially from the seeds of an African plant known as Griffonia simplicifolia 5-HTP is used for sleep disorders such as insomnia, depression, anxiety, migraine and tension-type headaches, fibromyalgia, obesity, premenstrual syndrome (PMS), premenstrual dysphoric disorder (PMDD), attention deficit-hyperactivity disorder (ADHD), seizure disorder, and Parkinson's disease..
Outside the brain, oxytocin-containing cells have been identified in several diverse tissues, including in females in the corpus luteum[34][35] and the placenta;[36] in males in the testicles' interstitial cells of Leydig;[37] and in both sexes in the retina,[38] the adrenal medulla,[39] the thymus[40] and the pancreas.[41] The finding of significant amounts of this classically "neurohypophysial" hormone outside the central nervous system raises many questions regarding its possible importance in these different tissues.

High and low oxytocin levels are possible, but research has not yet found any implications of these conditions. Men with high levels of oxytocin sometimes develop benign prostatic hyperplasia, or the enlarging of the prostate gland. This condition can cause urinary complaints. A lack of oxytocin can prevent the milk letdown reflex and make breastfeeding difficult. Low oxytocin levels have also been linked to depression, but using oxytocin to treat mental health conditions has not yet been studied sufficiently.
5-HTP is converted by the body to serotonin, a chemical in the brain that plays an important role in mood, sleep, and appetite. Many prescription medications used for the treatment of depression increase serotonin concentrations in the brain. Because of 5-HTP's pathway to serotonin, it has appealed to researchers as well as the public as a "natural" alternative to antidepressants and treatment of depression, insomnia, migraines, obesity, and fibromyalgia.
Do not fall for the easier methods of using MT-2, injections is the only proper way of using this peptide. Many Internet suppliers will sell things like nasal sprays, pre-mixed peptide, oral pills and powders, they simply don't work, if they did no one would use injections, right? There are a some positive reports of nasal spray experience, however its not very cost effective as peptide molecules in this form are large and difficult to pass the nasal membrance, there is some effect, but its minor comparable to injection route where absorption rate is 100%. Similarly, pills of this type are also quite useless because enzymes within the stomach will render the peptide inert.

A handful of large-scale clinical trials are now getting under way to test oxytocin and oxytocin-based therapies for autism spectrum disorder, and to work out who could benefit. Linmarie Sikich, a child psychiatrist at the University of North Carolina is heading the largest of these trials. Sikich plans to recruit 300 people with autism spectrum disorder, ranging in age from 3 to 17, and give them 6 months of either oxytocin or a placebo, followed by 6 months in which everyone will receive oxytocin.
When combined with antidepressants of the MAOI or SSRI class, very high parenteral doses of 5-HTP can cause acute serotonin syndrome in rats.[23][24] It is unclear if such findings have clinical relevance, as most drugs will cause serious adverse events or death in rodents at very high doses. In humans 5-HTP has never been clinically associated with serotonin syndrome, although 5-HTP can precipitate mania when added to an MAOI.[25]